Characterization and quantitation of foreign substances, secretions and cells which accumulate in airways and interstitium of persons exposed to foreign inhalants and who develop impaired pulmonary functions is in progress. These foreign materials include, in addition to amorphous carbon, several types of crystalline aluminum silicates as well as silica. A major environmental source of these soil-type inflammagens is cigarette smoke but other sources, not yet identified, exist since similar crystals are also found in alveolar macrophages of non-smokers. The toxic effect of these accumulated silicious materials, on isolated alveolar macrophages, cultured Type II cells and pulmonary fibroblasts are in progress. These silicates, when contaminated with cigarette smoke, cause peritoneal macrophages to become cytotoxic against transformed cultured human cells, but do not alter growth rates of human Type II cells or pulmonary fibroblasts.